Facultative intracellular pathogens, such as the causative agents of tuberculosis, leprosy, and leischmaniasis, continue to be a serious threat to human health. A valuable and widely used laboratory model for this type of host-pathogen interaction has been provided by experimental infection of mice with the facultative intracellular bacterium Listeria monocytogenes. It generally has been assumed that immunologically-activated macrophages are the only cells capable of killing L. monocytogenes. In contrast to this assumption, however, recent reports by this investigator have suggested that other cell types (i.e. inflammatory neutrophils and macrophages) also can kill L. monocytogenes, and that it is the ability of the host to efficiently mobilize inflammatory phagocytes to sites of listeria infection that is critical to the outcome of the disease. This hypothesis has been strengthened by subsequent experiments which have shown that Listeria-immune T cells can transfer both enhanced resistance to listeriosis and an increased ability to accumulate inflammatory neutrophils and macrophages. The purpose of this research will be to analyze how the inflammatory response contributes to resistance to listeriosis. To accomplish this goal the effects of cell number, route, and timing of administration of Listeria-immune T cells on the adoptive transfer of both enhanced resistance to listeriosis and increased inflammatory responsiveness will be determined, as will the Lyt phenotype of the T cells responsible for mediating these phenomena. Inbred mouse strains which vary in their levels of C5 will be used as a tool to identify the role of complement in both T cell-mediated resistance to listeriosis and enhanced inflammatory responsiveness. Direct evidence for the role of inflammation in resistance to listeriosis will be provided by in vivo experiments which will determine the effects of inflammation on the ability of L. monocytogenes to survive in vitro.